Evidence map›Paper›PMID 30429287›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2018

Complement Inhibitor CRIg/FH Ameliorates Renal Ischemia Reperfusion Injury via Activation of PI3K/AKT Signaling.

Chao Hu, Long Li, Peipei Ding, Ling Li, Xiaowen Ge, Long Zheng, Xuanchuan Wang, Jina Wang, Weitao Zhang, Na Wang and 6 more

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Chao HuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Long LiDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Peipei DingFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Collaborative Innovation Center of Cancer Medicine, Fudan University, Shanghai 200032, China.
Ling LiFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Collaborative Innovation Center of Cancer Medicine, Fudan University, Shanghai 200032, China.
Xiaowen GeDepartment of Pathology, Zhongshan Hospital, Fudan University, Shanghai 200032, China; and.
Long ZhengDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Xuanchuan WangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Jina WangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.ORCID 0000-0001-5357-9528
Weitao ZhangDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Na WangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Collaborative Innovation Center of Cancer Medicine, Fudan University, Shanghai 200032, China.
Hongyu GuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Collaborative Innovation Center of Cancer Medicine, Fudan University, Shanghai 200032, China.
Fan ZhongFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Collaborative Innovation Center of Cancer Medicine, Fudan University, Shanghai 200032, China.ORCID 0000-0001-9915-9609
Ming XuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Ruiming RongDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Tongyu ZhuDepartment of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China; weiguohu@fudan.edu.cn zhu.tongyu@zs-hospital.sh.cn.
Weiguo HuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Collaborative Innovation Center of Cancer Medicine, Fudan University, Shanghai 200032, China; weiguohu@fudan.edu.cn zhu.tongyu@zs-hospital.sh.cn.ORCID 0000-0002-7397-6800

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement activation is involved in the pathogenesis of ischemia reperfusion injury (IRI), which is an inevitable process during kidney transplantation. Therefore, complement-targeted therapeutics hold great potential in protecting the allografts from IRI. We observed universal deposition of C3d and membrane attack complex in human renal allografts with delayed graft function or biopsy-proved rejection, which confirmed the involvement of complement in IRI. Using

Indexed as

Kidney TransplantationAnimalsCells, CulturedComplement ActivationComplement C3dComplement Membrane Attack ComplexCytokinesDelayed Graft FunctionGraft RejectionHumansIsoantigensKidneyMiceMice, Inbred C57BLMice, KnockoutPhosphatidylinositol 3-KinasesComplement C3dComplement Membrane Attack ComplexCR1 protein, humanCytokinesIsoantigensPhosphatidylinositol 3-KinasesReceptors, Complement 3b

Identifiers

PMID30429287
PMCPMC6287101

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.